Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It had been previously thought that protein excretion in hypertensive nephrosclerosis was less than 0.5 to 1.0 g/24 h. Furthermore, it was believed that proteinuria in the nephrotic range associated with hypertension was probably due to primary renal disease, malignant hypertension, renal artery stenosis, or pheochromocytoma. We report eight patients with biopsy-proven hypertensive nephropathy and heavy proteinuria in the absence of malignant hypertension or renal artery stenosis. The 24-hour protein excretion ranged from 2.7 to 4.3 g. All patients had renal insufficiency, with serum creatinine ranging from 2.0 (176.8) to 7.8 mg/dL (689.5 mumol/L). Renal function worsened in most patients during the follow-up period despite adequate control of the hypertension, and three patients had to be started on hemodialysis. Three patients died during the follow-up period. We conclude that hypertensive nephrosclerosis must be included in the differential diagnosis of marked proteinuria in patients with essential hypertension and that heavy proteinuria, along with renal insufficiency, are poor prognostic indicators in such patients.
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PMID:Proteinuria in hypertension. 368 33

The occurrence of renal scleroderma (RSc) was sought retrospectively in 36 consecutive patients with scleroderma, seen in a single rheumatology unit, over a 12-year period. The diagnosis RSc was considered when at least one of the following findings was present: systolic blood pressure greater than or equal to 95 mmH, proteinuria greater than or equal to 0.5 gr/24 hr., and creatinine clearance less than or equal to 50 ml/min.: at least one of these features was found in 16 patients. Hypertension was the most frequent feature of RSc (15 out of 16 patients). Two forms of hypertension were observed. Firstly: malignant hypertension occurring early in the course of RSc, seen in 5 patients, 4 of whom rapidly developed terminal renal insufficiency. Secondly: a moderate hypertension, seen in 10 patients with a more favourable outcome, occurring on average 53 months after the diagnosis of scleroderma was made. Proteinuria was only seen in association with malignant hypertension. Renal impairment occurred in 7 patients. Of the 36 patients with scleroderma, 14 died; 10 of these 14 patients had RSc. Thus the death rate in patients with RSc was very high, whereas only 4 out of 20 died in the group without RSc.
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PMID:Renal scleroderma, value of clinical markers. 408 59

The patients with severe and 10 with accelerated or malignant hypertension were treated with the angiotensin-converting enzyme inhibitor captopril. Captopril acutely reduced blood pressure in all patients except two who had suppressed plasma renin activity. Four patients with encephalopathy showed immediate improvement after the first dose. Two patients could be withdrawn from nitroprusside infusion upon administration of captopril. Nineteen of 20 patients have remained on captopril for 12-32 months. Blood pressure is controlled in 18 and improved in two. Eleven required addition of diuretic and one addition of clonidine. The maximal antihypertensive effect of captopril with or without diuretics was evident after 3 months of continuous therapy and was associated with elevated plasma renin levels, normal aldosterone excretion and preservation of renal function. Captopril was well-tolerated, but produced occasional rash, loss of taste and proteinuria. We conclude that captopril, alone or in combination with other drugs, is effective in both the acute and long-term management of severe and malignant hypertension.
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PMID:Acute and chronic treatment of severe and malignant hypertension with the oral angiotensin-converting enzyme inhibitor captopril. 616 12

In order to determine the influence of hypertension on the progression of chronic glomerulonephritis, we studied the renal lesions in Heymann nephritis (autologous immune complex nephritis) produced in SHR. Nephritic SHR treated by AHD, normal SHR, nephritic WKYR, and normal WKYR served as controls. Induction of Heymann nephritis did not alter the blood pressure in either SHR or WKYR as compared with each untreated control group. Administration of AHD normalized the blood pressure of SHR. Proteinuria, hypoproteinemia, hypercholesterolemia, and reduction in body weight were significantly greater in nephritic SHR than in nephritic SHR treated by AHD or nephritic WKYR, whereas BUN and serum creatinine were unchanged in all the nephritic rats. Histological findings such as glomerular basement membrane thickening, IgG and C3 deposits along capillary walls, and subepithelial electron-dense deposits were similar in all nephritic groups. Glomerular sclerosis and tubulointerstitial changes were more marked in nephritic SHR than in the other nephritic groups. Severe vascular thickening and necrosis, intravascular thrombosis, and perivascular cell infiltration were frequently observed in nephritic SHR. These lesions are characteristic of malignant hypertension. However, they were not found in control SHR, which maintained elevation of blood pressure equivalent to that of nephritic SHR throughout the study. It was concluded that hypertension may aggravate nephritic manifestations such as proteinuria, hypoproteinemia, and hypercholesterolemia but not excretory renal function and that the hypertensive vascular lesions are augmented by Heymann nephritis.
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PMID:Influence of hypertension on the progression of experimental autologous immune complex nephritis. 621 70

Renal biopsies were carried out in 29 patients with scleroderma to study the early vascular lesions and their eventual clinical significance. Haemolytic acute renal failure was present in 9 patients. The biopsies showed early vascular lesions on interlobar arteries. The main biological change was proliferative or fibrous endarteritis. Mucoid infiltration was found in 3 biopsies. The arterioles were spared or only slightly affected without major fibrinoid necrosis. These lesions were therefore distinct from those of malignant hypertension. However, at autopsy of 2 of these cases, the vascular lesions were undistinguishable from those of malignant hypertension. The biopsies in 13 out of 14 patients with scleroderma without obvious renal involvement (9 cases) or with moderate proteinuria and/or hypertension without renal failure (5 cases) showed interlobar endarteritis with associated mucoid infiltration in 3 patients. This lesion was isolated but sometimes extensive even in young patients without hypertension. One patient died within one year, of disseminated colonic carcinoma, and 4 of cardio-respiratory failure due to scleroderma without hypertension, renal failure or proteinuria. Eight of the 9 remaining patients were traced 6 to 16 years after biopsy. Two were moderately hypertensive but none had renal failure. Cutaneous and internal organ scleroderma had regressed in the majority and proteinuria had disappeared in 3 cases.
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PMID:[Renal involvement in scleroderma]. 652 54

IgA-glomerulonephritis represents the most frequent glomerulonephritis (GN; 20%) among our patients. In contrast to data from the literature the prognosis is not benign. Renal insufficiency developed in 17 out of 50 investigated patients within 4 to 96 months, 3 of these patients had to undergo dialysis. Eleven of the 17 patients still had a normal renal function at the time of diagnosis. Malignant hypertension was present in 5 patients. An unfavourable course was predictable in cases of male gender, proteinuria, hypertension, age above 30 years, and histological changes indicating glomerulosclerosis, tubular atrophy, interstitial fibrosis and vascular lesions. Increased serum IgA levels, circulating IgA complexes, association with certain HLA-B or -Dr antigens as well as clinical symptoms and signs of haematuria, dysuria and kidney pains were not helpful either for diagnosis or for prognosis. The value of skin biopsy was comparatively small. Positive IgA demonstration was possible in 12 out of 41 cases with IgA-GN, however, also in 4 out of 21 patients with non-IgA-GN. None of 50 probands without renal disease showed IgA. Five out of 7 skin biopsies demonstrated IgA2, one IgA1 and one both IgA1 and IgA2. Increased serum IgA levels were found in a high percentage (21 out of 38 patients). The same applied to circulating IgA-complexes (8 out of 33 patients).
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PMID:[Mesangial IgA-glomerulonephritis]. 682 88

1 Analgesic nephropathy is part of the analgesic syndrome which has gastrointestinal, haematological, cardiovascular, psychological and psychiatric, and pregnancy and gonadal manifestations; premature ageing may also be a feature. 2 Analgesic nephropathy is a form of renal disease characterized by renal papillary necrosis, secondary chronic interstitial nephritis and renal failure with features of predominant tubulointerstitial dysfunction. 3 The percentage of patients with analgesic nephropathy who present with terminal renal failure is 12%. With appropriate management, 17% of analgesic nephropathy patients improve, 50% remain stable and 23% deteriorate. The 6 year cumulative survival is 70%. The major factors influencing deterioration are malignant hypertension, persistent proteinuria and small initial renal size. 4 The risk of renal papillary carcinoma in patients who regularly take analgesics is 8 per 100,000 patients per year. 5 Renal papillary necrosis is a consequence of the chronic toxicity of all non-steroidal anti-inflammatory drugs and results from medullary ischaemia secondary to suppression of prostaglandin E2 synthesis and from direct cellular toxicity. 6 Analgesic nephropathy is a preventable form of renal disease and renal failure. It can be prevented by limiting the abuse potential of analgesics rather than by making minor modifications in the composition of analgesic mixtures.
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PMID:Clinical and pathological aspects of analgesic nephropathy. 700 90

Of 58 patients treated with captopril, 3 have now received the drug for more than 2 years and 22 for more than one year. This study concerns 38 patients treated for 6 months, captopril having been given alone during the first 2 months. They all had severe hypertension (diastolic BP Greater Than 110 mmHg) which had resisted previous treatments in normally effective doses, including at least one beta-blocker, dihydralazine and a diuretic. After 6 months blood pressure levels were normal in 53% of the patients, reduced in 31% and unchanged in 16%. Clinical improvement was habitual with, in particular, disappearance or decrease of tiredness and dyspnoea. Since some side-effects of the drug, such as granulopenia, proteinuria and ageusia, are mainly observed with high dosage, captopril is usually administered in doses lower or equal to 400 mg/day. In resistant or malignant hypertension it must be used in combination with salt-free diet, a beta-blocker and/or prazosin. Clinical, haematological and renal surveillance is necessary during treatment. When these precautions are observed, captopril constitutes a very useful drug for the treatment of patients with severe resistant hypertension.
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PMID:[Treatment of severe resistant arterial hypertension with captopril. 58 patients, including 38 treated for more than 6 months (author's transl)]. 702 47

An unusual familial glomerular disease, characterized by the presence of diffuse round mesangial deposits of C3, is described in 2 siblings (1 male and 1 female) and their mother. The clinical picture in the 3 patients was a long-lasting proteinuria. An acute hemolytic uremic syndrome with malignant hypertension developed in the male at the age of 24 years, requiring bilateral nephrectomy. The glomerulonephritis recurred on a renal allograft. This disease is not HLA-linked and no characteristic abnormality of complement profile was seen in the 3 patients.
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PMID:A new form of familial glomerulonephritis. 704 14

A twenty-one-year-old male was admitted to our hospital because of hypertension and proteinuria. He had felt general fatigue and low grade fever for one month. Blood pressure was 180/120 mmHg on admission. Laboratory findings showed 3+ proteinuria and 1+ occult blood in urinalysis; an accelerated erythrocyte sedimentation rate (ESR) of 39 mm/hr; elevation of LDH to 755 IU/l. Antinuclear antibody was positive with a titer of 1: 160, with a speckled pattern. Plasma renin activity and serum aldosterone were markedly elevated to 25.8 ng/ml/hr and 585.3 pg/ml, respectively. Renal function had declined mildly; endogenous creatinine clearance was 60 ml/min. Renal arteriogram demonstrated multiple intrarenal aneurysms in the bilateral kidneys. Aneurysms, 5-8 mm in diameter were located in the arteries from the interlobar to interlobular region. He was diagnosed as having polyarteritis nodosa (PN) and was then treated with 20 mg/day of prednisolone and monthly pulse therapy of cyclophosphamide. After steroid, cyclophosphamide and anti-hypertensive therapy, he became well and had normal blood pressure. The patient was considered a rare case of PN with multiple intrarenal aneurysms and accelerated hypertension. We discuss aneurysms in PN and accelerated or malignant hypertension documented in the literature.
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PMID:[A case of polyarteritis nodosa presenting with multiple intrarenal aneurysms and accelerated hypertension]. 769 55


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